MicroRNA‑32 promotes ovarian cancer cell proliferation and motility by targeting SMG1
- Saitian Zeng
- Shikai Liu
- Jing Feng
- Jiefan Gao
- Fengxia Xue
Affiliations: Department of Gynecology and Obstetrics, Tianjin Medical University General Hospital, Tianjin 300052, P.R. China, Department of Gynecology and Obstetrics, Cangzhou Central Hospital, Hebei Medical University, Cangzhou, Hebei 061000, P.R. China
- Published online on: May 14, 2020 https://doi.org/10.3892/ol.2020.11624
Copyright: © Zeng
et al. This is an open access article distributed under the
terms of Creative
Commons Attribution License.
Views: 0 (Spandidos Publications: | PMC Statistics: )
Total PDF Downloads: 0 (Spandidos Publications: | PMC Statistics: )
This article is mentioned in:
Ovarian cancer (OC) is the most lethal gynecological malignancy and one of the leading causes of cancer‑related deaths among women. Metastasis is the main cause of poor prognosis in OC. MicroRNA (miRNA/miR) has been shown to play an important role in tumorigenesis and metastasis in various cancer types by affecting the expression of its targets. In the present study, the role of miR‑32 (miR‑32‑5p) in OC was explored. Reverse transcription‑quantitative PCR results showed that miR‑32 expression was significantly upregulated in both OC tissues and cell lines. Inhibition of miR‑32 by transfection with miR‑32 inhibitor in OC cells markedly suppressed cell proliferation, migration and invasion. In addition, a luciferase assay showed that suppressor of morphogenesis in genitalia 1 (SMG1) is a direct target of miR‑32, and interference in SMG1 expression with transfection of SMG1 small hairpin RNA restored miR‑32‑mediated OC cell proliferation, migration and invasion. Taken together, these results indicate that miR‑32 may promote OC cell growth and motility by targeting SMG1. The data of the present study suggest that miR‑32 may serve as a potential therapeutic target for OC treatment in the future.